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Differential cardiac effects in rats exposed to atmospheric smog generated from isoprene versus toluene
Hazari, M., K. Stratford, Todd Krantz, C. King, J. Krug, L. Thompson, A. Farraj, AND Ian Gilmour. Differential cardiac effects in rats exposed to atmospheric smog generated from isoprene versus toluene. Society of Toxicology 2017, Baltimore, MD, March 12 - 16, 2017.
The purpose of this study was to compare the cardiac effects of smog generated from isoprene versus toluene. These data demonstrate that smog generated from different sources have varying toxicities and effects on the heart.
The results of this study demonstrate that atmospheric smog generated from both isoprene and toluene cause cardiac effects in rats. In addition, it appears that smog from toluene is more toxic in terms of cardiac arrhythmogenicity. Smog, which is a complex mixture of particulate matter and gaseous irritants (ozone, sulfur dioxide, reactive aldehydes), as well as components which react with sunlight to form secondary pollutants, has recently been linked to increased risk of adverse cardiac responses. The components, and therefore health effects, of atmospheric smog are determined by the fuel used to generate them. In this study we examined the difference between isoprene- and toluene-generated smog in causing cardiac effects in rats and hypothesized that both atmospheres would cause cardiac electrical and functional changes in rats. Male Wistar-Kyoto rats were exposed to either atmospheric smog generated by the USEPA’s mobile reaction chamber using either isoprene or toluene, or filtered air for four hours. One day later, rats were anesthetized and left ventricular functional responses to dobutamine were measured using a Millar probe and arrhythmia sensitivity to aconitine. Baseline left ventricular pressure (LVP) was lower in toluene-exposed animals but not isoprene when compared to air. Increases in LVP with increasing doses of dobutamine were impaired only in toluene-exposed rats. Both isoprene and toluene impaired the rate of ventricular relaxation (dP/dTmin) during administration of dobutamine whereas contractility (dP/dTmax) was not significantly different. Finally, toluene significantly increased aconitine-induced arrhythmia whereas isoprene only showed a trend. The results of this study show that a single exposure to either isoprene- or toluene-generated smog causes acute cardiac effects in rats. Although the functional responses likely do not represent serious or permanent underlying deficits, it is clear that smog derived from toluene is far more potent in causing arrhythmia than isoprene. (This abstract does not reflect USEPA policy)